Inhibition of Galectin-3 Prevents New Blood Vessel Formation

Studies on the relationship between the carbohydrate-binding protein galectin-3 and angiogenesis have revealed several new potential targets for drugs to inhibit the generation of new blood vessels that enables tumors to grow and spread.

Previous research had shown that galectin-3 was a novel proangiogenic molecule, but the mechanism by which galectin-3 promoted angiogenesis was unknown. Now, investigators at the Tufts University School of Medicine (Boston, MA, USA) have used a series of biochemical and genomic tools to establish how galectin-3 influences the process of angiogenesis.

They reported in the August 16, 2010, online edition of the Journal of Experimental Medicine that galectin-3 inhibitors as well as antibodies against the galectin-3 binding protein integrin alpha-v-beta-3 blocked angiogenesis in a mouse model. Similarly, angiogenesis was inhibited in mice genetically engineered to lack the galectin-3 gene. Stimulation of angiogenesis by galectin-3 was ultimately linked to its effect on the endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF)-mediated molecular pathway.

"Our study shows that galectin-3 protein binds to glycans (carbohydrate portions) of specific cell-adhesion proteins, the integrins, to activate the signaling pathways that bring about angiogenesis. This improved understanding may provide a more targeted approach to preventing harmful angiogenesis,” said senior author Dr. Noorjahan Panjwani, professor of ophthalmology at Tufts University Medical School. "By deciphering the mechanism of galectin-3 action, we were able to establish more than one therapeutic target. The more we know about how this pathway works, the more options we have for potential treatments.”


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